Abstract
With the aging population on the rise, the higher prevalence of atrial tachyarrhythmia is emerging as a significant healthcare concern. Atrial fibrillation (AF) stands out as the most common atrial tachyarrhythmia, potentially leading to adverse outcomes, such as stroke, heart failure (HF), or conduction dysfunction. Furthermore, AF may serve as a manifestation of underlying atrial cardiomyopathy, which forms the structural and electrical substrate for arrhythmias. Atrial cardiomyopathy is characterized by structural and electrical remodeling of the atria, resulting in impaired mechanical function and the generation of arrhythmias. Sodium-glucose cotransporter 2 inhibitors (SGLT2is) have recently emerged as a novel medical treatment for HF. Their use has been associated with a reduced incidence of new-onset AF, potentially attributing to the improvement of atrial cardiomyopathy. This effect is achieved through the regulation of glucose utilization and energy consumption within the myocardium. It is worth noting that the sirtuin signaling pathway plays a crucial role in regulating energy consumption, especially in the presence of increased oxidative stress and fibrosis. This pathway also exerts a significant influence on various cardiovascular diseases. This review aims to provide a comprehensive summary of the involvement of the sirtuin signaling pathway in cardiovascular diseases, with a specific focus on atrial cardiomyopathy and AF and the potential molecular mechanisms of SGLT2is in the sirtuin signaling pathway and atrial cardiomyopathy.
Keywords: Sirtuin signaling pathway, atrial cardiomyopathy, atrial fibrillation, sodium–glucose cotransporter 2 inhibitors, fibrosis
